Cognitive decline and memory problems are a prominent feature of so-called "normal" aging. However, some would argue that this memory loss is not normal, and should be addressed as an early disease state. Across the adult life span, the process of learning new information and storing permanent memories becomes more and more difficult, and often fails entirely. Storing information alters the functionality of neurons through many mechanisms. One of these pathways is altering the excitability of the cell. Reduced neuronal excitability could be responsible for an inability to receive and store new information. The AHP and slow AHP currents have previously been implicated in learning and age-related learning deficits. Another faster potassium current named Ic, or fAHP is known to be both voltage and calcium dependent. Because previous reports have shown that the involvement of the AHP in learning is altered over time, it is expected that older subjects will have an altered Ic current when compared to younger adults, contributing to age-related learning deficits. This study proposes to examine the fast AHP current, Ic, and its relationship to somatic excitability after learning and alterations in this current caused by normal aging. [unreadable] [unreadable] [unreadable]